Support is requested for a scientific meeting organized by the American Association for Cancer Research, Inc. (AACR). The meeting, to be held at the Banff Springs Hotel from February 19 to February 24, 1994, will focus on new and exciting findings on the cell cycle, mutations, and chromosomal stability. Our goal is to bring together three groups of scientists who investigate basic molecular mechanisms causally associated with human cancer. We are interested in the interrelationships among cellular responses to DNA damage, cell cycle control, and genetic instability. The conference will be organized by Dr. Thea D. Tlsty, Associate Professor in the Department of Pathology at the Lineberger Comprehensive Cancer Center, University of North Carolina, and Dr. Lawrence A. Loeb, Professor in the Departments of Pathology and Biochemistry at the University of Washington. There will be nine formal sections with oral presentations, and three with poster presentations. Each of the speakers has made seminal contributions to our knowledge of chromosomal stability and human cancer. We anticipate 225 to 250 registrants, many of whom will have the opportunity to discuss their research during the poster sessions. The scope of presentations will span topics ranging from endogenous sources of DNA damage, spontaneous mutations, cell cycle controls, and mechanisms that guarantee genetic stability. The principal focus of the conference is the role of the cell cycle in controlling genetic stability in normal cells and alterations in these cellular pathways leading to mutations, gene amplification, and human cancer. Using new techniques in molecular biology, it has now become feasible to define the cellular mechanisms that control DNA replication, chromosomal segregation and division at the molecular and perhaps even atomic level. Genes that control these central biological processes are being rapidly isolated m organisms from yeast to humans. The products of these genes are being identified, purified, and characterized. This revolution in our knowledge about the cell cycle has allowed us to begin to define how one cell becomes two. One can now ask why malignant cells are able to divide in situations in which normal cells do not. Why are chromosomal abnormalities characteristic of malignancy? How many mutations occur during the course of malignancy, and which genes are mutated? By assembling scientists in these different disciplines, we hope to stimulate new ideas, new approaches, and key critical experiments. We are confident that the exchange of ideas among leading scientists working in these areas of investigation will stimulate new and original ideas that will contribute to progress in cancer research.